Evidence map›Paper›PMID 28186192›Full record

ArticleScientific reports2017

Reduced Necrosis and Content of Apoptotic M1 Macrophages in Advanced Atherosclerotic Plaques of Mice With Macrophage-Specific Loss of Trpc3.

Sumeet Solanki, Prabhatchandra R Dube, Lutz Birnbaumer, Guillermo Vazquez

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.0field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 34 citations in OpenAlex.

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  15. Modulation of Peripheral CD4Frontiers in cardiovascular medicine · 2021
    Article
  16. Article
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  18. TRPC and TRPV Channels' Role in Vascular Remodeling and Disease.International journal of molecular sciences · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Sumeet SolankiDepartment of Physiology and Pharmacology, and Center for Hypertension and Personalized Medicine, University of Toledo College of Medicine and Life Sciences, University of Toledo Health Science Campus, 3000 Transverse Dr., Toledo, Ohio 43614, USA.
Prabhatchandra R DubeDepartment of Physiology and Pharmacology, and Center for Hypertension and Personalized Medicine, University of Toledo College of Medicine and Life Sciences, University of Toledo Health Science Campus, 3000 Transverse Dr., Toledo, Ohio 43614, USA.
Lutz BirnbaumerNeurobiology Laboratory, National Institute of Environmental Health Sciences, 111 TW Alexander Dr., Research Triangle Park, North Carolina 27709, USA.
Guillermo VazquezDepartment of Physiology and Pharmacology, and Center for Hypertension and Personalized Medicine, University of Toledo College of Medicine and Life Sciences, University of Toledo Health Science Campus, 3000 Transverse Dr., Toledo, Ohio 43614, USA.
University of Toledo · USNational Institute of Environmental Health Sciences · US

Funding

TRPC3 Channels in Molecular and Cellular Events of AtherogenesisR01HL111877 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI VAZQUEZ, GUILLERMO · 2012 to 2015
$1.5M
Protein Microcharacterization FacilityZ01ES101564 · NIEHS · ENVIRONMENTAL HEALTH SCIENCES · PI TOMER, KENNETH · 2003 to 2007
$685k
"Novel roles of the TRPC3 channel in macrophage functions: implications in atherosclerosis"R56HL125619 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI VAZQUEZ, GUILLERMO · 2016 to 2016
$379k
NHLBI NIH HHS R01 HL111877NHLBI NIH HHS R56 HL125619NIEHS NIH HHS Z01 ES101564
6 · The paper itself

Abstract

In previous work we reported that ApoeKO mice transplanted with bone marrow cells deficient in the Transient Receptor Potential Canonical 3 (TRPC3) channel have reduced necrosis and number of apoptotic macrophages in advanced atherosclerotic plaques. Also, in vitro studies with polarized macrophages derived from mice with macrophage-specific loss of TRPC3 showed that M1, but not M2 macrophages, deficient in Trpc3 are less susceptible to ER stress-induced apoptosis than Trpc3 expressing cells. The questions remained (a) whether the plaque phenotype in transplanted mice resulted from a genuine effect of Trpc3 on macrophages, and (b) whether the reduced necrosis and macrophage apoptosis in plaques of these mice was a manifestation of the selective effect of TRPC3 on apoptosis of M1 macrophages previously observed in vitro. Here, we addressed these questions using Ldlr knockout (Ldlr

Indexed as

AnimalsApoptosisAtherosclerosisBiomarkersDisease Models, AnimalFemaleImmunohistochemistryMacrophagesMiceMice, KnockoutNecrosisPlaque, AtheroscleroticReceptors, LDLTRPC Cation ChannelsBiomarkersReceptors, LDLTRPC3 cation channelTRPC Cation Channels

Identifiers

PMID28186192
PMCPMC5301208
OpenAlexW2587045254

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.